[Show abstract][Hide abstract] ABSTRACT: Venous stenosis is a significant problem in arteriovenous fistulae, likely due to anatomical configuration and wall shear stress profiles. To identify linkages between wall shear stress and the magnitude and pattern of vascular stenosis, we produced curved and straight fistulae in a pig model. A complete wall stress profile was calculated for the curved configuration and correlated with luminal stenosis. Computer modeling techniques were then used to derive a wall shear stress profile for the straight arteriovenous fistula. Differences in the wall shear stress profile of the curved and straight fistula were then related to histological findings. There was a marked inverse correlation between the magnitude of wall shear stress within different regions of the curved arteriovenous fistula and luminal stenosis in these same regions. There were also significantly greater differences in wall shear stress between the outer and inner walls of the straight as compared to curved arteriovenous fistula, which translated into a more eccentric histological pattern of intima-media thickening. Our results suggest a clear linkage between anatomical configuration, wall shear stress profiles, and the pattern of luminal stenosis and intima-media thickening in a pig model of arteriovenous fistula stenosis. These results suggest that fistula failure could be reduced by using computer modeling prior to surgical placement to alter the anatomical and, consequently, the wall shear stress profiles in an arteriovenous fistula.Keywords: AV fistula configuration, computational fluid dynamics, hemodialysis vascular access dysfunction, hemodynamics, wall shear stress
Kidney International 09/2008; 74(11):1410-1419. · 8.52 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The severity of epicardial coronary stenosis can be assessed by invasive measurements of trans-stenotic pressure drop and flow. A pressure or flow sensor-tipped guidewire inserted across the coronary stenosis causes an overestimation in true trans-stenotic pressure drop and reduction in coronary flow. This may mask the true severity of coronary stenosis. In order to unmask the true severity of epicardial stenosis, we evaluate a diagnostic parameter, which is obtained from fundamental fluid dynamics principles. This experimental and numerical study focuses on the characterization of the diagnostic parameter, pressure drop coefficient, and also evaluates the pressure recovery downstream of stenoses.
Three models of coronary stenosis namely, moderate, intermediate and severe stenosis, were manufactured and tested in the in-vitro set-up simulating the epicardial coronary network. The trans-stenotic pressure drop and flow distal to stenosis models were measured by non-invasive method, using external pressure and flow sensors, and by invasive method, following guidewire insertion across the stenosis. The viscous and momentum-change components of the pressure drop for various flow rates were evaluated from quadratic relation between pressure drop and flow. Finally, the pressure drop coefficient (CDPe) was calculated as the ratio of pressure drop and distal dynamic pressure. The pressure recovery factor (eta) was calculated as the ratio of pressure recovery coefficient and the area blockage.
The mean pressure drop-flow characteristics before and during guidewire insertion indicated that increasing stenosis causes a shift in dominance from viscous pressure to momentum forces. However, for intermediate (approximately 80%) area stenosis, which is between moderate (approximately 65%) and severe (approximately 90%) area stenoses, both losses were similar in magnitude. Therefore, guidewire insertion plays a critical role in evaluating the hemodynamic severity of coronary stenosis. More importantly, mean CDPe increased (17 +/- 3.3 to 287 +/- 52, n = 3, p < 0.01) and mean eta decreased (0.54 +/- 0.04 to 0.37 +/- 0.05, p < 0.01) from moderate to severe stenosis during guidewire insertion.
The wide range of CDPe is not affected that much by the presence of guidewire. CDPe can be used in clinical practice to evaluate the true severity of coronary stenosis due to its significant difference between values measured at moderate and severe stenoses.
[Show abstract][Hide abstract] ABSTRACT: One of the commonly used parameters for evaluating aortic regurgitation is the rate of pressure decay data obtained from echocardiographic evaluation or cardiac catheterization. The measurement of the rate of equalization of pressure between the aorta and the left ventricle and its utility in the setting of aortic insufficiency has been validated. Intuitively, the Doppler equivalent, pressure half-time, is inversely related to the severity of regurgitation. However, this is a phenomenon dependent on multiple variables including blood pressure, heart rate, compliance of the receiving chamber, effects of vasopressors and the volume status of the patient. We report a case of unique hemodynamics obtained during cardiac catheterization due to low filling pressures that was further confounded by elevated systemic vascular resistance in a critically ill patient with angiographically severe aortic regurgitation.
The Journal of invasive cardiology 06/2008; 20(6):E183-6. · 1.57 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Although arteriovenous fistulae (AVFs) are currently the preferred mode of permanent hemodialysis access they do have significant problems due to initial non-maturation and a later venous stenosis. These problems appear to have been exacerbated following a push to increase AVF prevalence in the US. The reasons for both AVF non-maturation and the later venous stenoses are unclear but are thought to be related to abnormal hemodynamic wall shear stress (WSS) profiles. This technical note aims to describe the successful development of measurement techniques that can be used to establish a complete hemodynamic profile in a pig model with two different configurations of AVF.
The curved and straight AVF configurations were created in an in vivo pig model. Flow and pressure in the AVFs were measured using the perivascular flow probes and Doppler flow wires while the pressure was recorded using a pressure transducer. The anatomical configuration was obtained using two different approaches: a) combination of intravascular ultrasound (IVUS) and angiograms, (b) 64 slice CT angiography. 3D models were reconstructed using image processing and computer modeling techniques. Numerical calculations were then performed by applying the measured flow and pressure data into the configurations to obtain the hemodynamic WSS profiles.
The described methodologies will allow the calculation and optimization of WSS profiles in animal models. This information could then be translated to the clinical setting where it would have a positive impact on improving the early maturation rates of AVFs as well as reducing the late venous stenoses.
The journal of vascular access 01/2008; 9(1):28-34. · 0.97 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Functional/physiological evaluation of coronary artery stenoses may be more important than anatomical measurements of severity. Optimization of thresholds for stenosis intervention and treatment endpoints depend on coupling functional hemodynamic and anatomical data. We sought to develop a single prognostic parameter correlating stenosis-specific anatomy, pressure gradient, and velocities that could be measured during catheterization.
In vivo Experiments were performed in six swine (41 +/- 3 kg). The lumen area of the left anterior descending coronary artery was measured with intravascular ultrasound. An angioplasty balloon was inflated to create the desired intraluminal area obstructions. Fractional flow reserve (FFR), coronary flow reserve (CFR), and hyperemic-stenosis-resistance index were measured distal to the balloon at peak hyperemia with 10 mg intracoronary papaverine. A functional index:pressure drop coefficient (CDP) and a combined functional and anatomical index:lesion flow coefficient (LFC) were calculated from measured hyperemic pressure gradient, velocity, and percentage area stenosis. P < 0.05 was considered statistically significant.
The CDP and LFC correlated linearly and significantly with FFR and CFR. The CDP (R(2) = 0.72, P < 0.0001) correlated better than LFC (R(2) = 0.19, P < 0.003) with hyperemic-stenosis-resistance index. When LFC was correlated simultaneously with FFR and CFR, R(2) improved to 0.82 (P < 0.0001). Inclusion of percentage area stenoses concurrently with FFR and CFR marginally improved the correlation with LFC.
A dimensionless parameter combining measured pressure gradient, velocity, and area reduction data can optimally define the severity of coronary stenoses based on our preliminary results and could prove useful clinically.
Journal of Surgical Research 11/2007; 150(1):24-33. · 2.02 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Myocardial fractional flow reserve (FFR(myo)) and coronary flow reserve (CFR), measured with guidewire, and quantitative angiography (QA) are widely used in combination to distinguish ischemic from non-ischemic coronary stenoses. Recent studies have shown that simultaneous measurements of FFR(myo) and CFR are recommended to dissociate conduit epicardial coronary stenoses from distal resistance microvascular disease. In this study, a more comprehensive diagnostic parameter, named as lesion flow coefficient, c, is proposed. The coefficient, c, which accounts for mean pressure drop, Delta p, mean coronary flow, Q, and percentage area stenosis, can be used to assess the hemodynamic severity of a coronary artery stenoses. Importantly, the contribution of viscous loss and loss due to momentum change for several lesion sizes can be distinguished using c. FFR(myo), CFR and c were calculated for pre-angioplasty, intermediate and post-angioplasty epicardial lesions, without microvascular disease. While hyperemic c decreased from 0.65 for pre-angioplasty to 0.48 for post-angioplasty lesion with guidewire of size 0.35 mm, FFR(myo) increased from 0.52 to 0.87, and CFR increased from 1.72 to 3.45, respectively. Thus, reduced loss produced by momentum change due to lower percentage area stenosis decreased c. For post-angioplasty lesion, c decreased from 0.55 to 0.48 with the insertion of guidewire. Hence, increased viscous loss due to the presence of guidewire decreased c compared with a lesion without guidewire. Further, c showed a linear relationship with FFR(myo), CFR and percentage area stenosis for pre-angioplasty, intermediate and post-angioplasty lesion. These baseline values of c were developed from fluid dynamics fundamentals for focal lesions, and provided a single hemodynamic endpoint to evaluate coronary stenosis severity.
Journal of Biomechanics 02/2007; 40(3):652-62. · 2.72 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Hemodynamic analysis was conducted to determine uncertainty in clinical measurements of coronary flow reserve (CFR) and fractional flow reserve (FFR) over pathophysiological conditions in a patient group with coronary artery disease during angioplasty. The vasodilation-distal perfusion pressure (CFR-p(rh)) curve was obtained for 0.35- and 0.46-mm guide wires. Our hypothesis is that a guide wire spanning the lesions elevates the pressure gradient and reduces the flow during hyperemic measurements. Maximal CFR-p(rh) was uniquely determined by the intersection of measured CFR and calculated p(rh) of native and residual epicardial lesions in patients without microvascular disease, during angioplasty. Extrapolation of the linear curve gave a zero-coronary flow mean pressure (p(zf)) of approximately 20 mmHg and a corresponding p(rh) of 55 mmHg in the native lesions, which coincided with the level that causes ischemia in human hearts. On this linear curve, values of CFR and FFRmyo (pathophysiological condition) and CFRg and FFRmyog (in the presence of the guide wire) were obtained in native and residual lesions. A strong linear correlation was found between CFR and CFRg [CFR = CFRg x 0.689 + 1.271 (R2= 0.99) for 0.46 mm and CFR = CFRg x 0.757 + 1.004 (R2= 0.99) for 0.35 mm] and between FFRmyo and FFRmyog [FFRmyo = FFRmyog x 0.737 + 0.263 (R2= 0.99) for 0.46 mm and FFRmyo = FFRmyog x 0.790 + 0.210 (R2= 0.99) for 0.35 mm]. This study establishes a strong correlation between CFR and CFRg and between FFRmyo and FFRmyog, which could be used to obtain the true state of occlusion in the coronary artery during angioplasty.